Extensive sensory testing of patients before and after oral extraction of lower third molar tooth showed that postoperative inflammation increased only the sensitivity of A beta touch afferents without effect on smaller, nociceptive afferents. Similar increases in sensitivity were found in three separate animal models of 1) tissue inflammation, 2) nerve inflammation and 3) nerve injury. Nerve Growth Factor (NGF) antiserum and pre-immune serum modulated the increased sensitivity. These results indicate that neural inflammation evokes central processes, mediated in part by NGF, that alter the sensitivity of A beta fibers that mediate fine touch, but do not alter the sensitivity of A delta and C fibers that mediate pain sensation. A fifth study evaluated the central effects of brief and tonic pain stimuli positron emission tomography (PET). Brief painful heat stimuli activated brain areas observed in previous studies. Ischemic pain, although severe, produced no significant brain activation. Post ischemia dysathesias produced a profound activation of areas involved in both sensory and affective processing. These studies both question the relevance of brief-stimuli activation to brain processing of chronic clinical pain, and provide the first observation of cerebral response to dysathetic pain, which is a common feature of neuropathic pain syndromes.